Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in hemostatic parameters following open-heart surgery with cardiopulmonary bypass were studied in twelve patients for two postoperative weeks. No clinical manifestations of hemostatic abnormalities were found in these patients throughout the study period. The prothrombin time and activated partial thromboplastin time were within normal limits. The platelet counts and fibrinogen levels were depleted on the first postoperative day, followed by a rapid return to above normal levels within 7 days. The fibrinogen/fibrin degradation products (FDP) showed a peak elevation on the first day, followed by a gradual decline. In 92% of the patients, the FDP levels became elevated to more than 10 micrograms/ml. Rate of the increase in FDP level was closely reflected by the amount of postoperative blood loss when the loss exceeded 10 ml/kg of body weight during 48 hours postoperatively. The levels of plasmin inhibitors (alpha 1-antitrypsin and alpha 2-macroglobulin) were also measured. the alpha 1 antitrypsin was elevated during the postoperative period. The alpha 2-macroglobulin showed no significant changes. In summary, the hemostatic changes following open-heart surgery included activation of the fibrinolytic system and depletion of coagulation factors immediately after surgery, followed by hypercoagulability due to a rapid return to above normal levels of coagulation factors and plasmin inhibitors. We consider, however, these changes to be part of the homeostatic response following open-heart surgery.
J Cardiovasc Surg (Torino)
PMID:Late changes in hemostatic parameters following open-heart surgery. 618 1

We retrospectively compared preoperative prothrombin (PT), partial thromboplastin (PTT), dilute whole blood clot lysis and bleeding times, fibrinogen level, and platelet count with subsequent blood component administration in 92 patients who had undergone cardiac operations with cardiopulmonary bypass (CPB). Abnormal results for one or more tests were found in 34% of 71 adults and 81% of 21 children and teenagers. The patients with abnormal test(s) received no more whole blood and packed red cell units, platelets, or plasma than those with normal tests in either age group. No individual or multiple test abnormalities predicted excess blood component transfusion, even when low-grade abnormalities were excluded. The high rate of abnormal tests in patients less than 20 years of age was not due to polycythemia and may indicate a need for age-specific reference ranges. Baseline PT, PTT, and platelet count may aid in the evaluation of the potential for subsequent development of coagulopathy, but we conclude that further preoperative testing may be reserved for infants, polycythemic individuals, or others in whom history or drug use suggests potential bleeding problems.
J Thorac Cardiovasc Surg 1983 Apr
PMID:Do preoperative laboratory tests predict blood transfusion needs in cardiac operations? 660 Dec 13

The use of a fixed dosage schedule was compared with the use of activated clotting time (ACT) for monitoring heparin anticoagulation and its neutralization during and after extracorporeal circulation in patients undergoing coronary artery bypass grafting. Use of ACT resulted in a statistically significant decrease in heparin and protamine dosages and statistically significant reductions in postoperative blood loss and blood transfusion needs. Postoperative levels of blood hemoglobin concentration were significantly higher and the activated partial thromboplastin time was significantly shorter with ACT monitoring than with use of a fixed dosage schedule. The results confirmed the superiority of the ACT method for monitoring anticoagulation during cardiac surgery.
Scand J Thorac Cardiovasc Surg 1984
PMID:Use of activated clotting time to monitor anticoagulation during cardiac surgery. 660 29

Thirty-four dogs underwent total cardiopulmonary bypass for 1 or 2 hours with a bubble oxygenator and cardiotomy suction. The dogs were divided into three groups: control dogs which received heparin alone, dogs which received prostacyclin (PGI2) and heparin, and dogs which received prostacyclin alone. PGI2 was given as a bolus (6 to 60 microgram) and then as a constant infusion (0.2 to 0.8 microgram/kg/min) in the venous outflow line. The pump flows were equal in the three groups. PGI2 as a bolus led to transient hypotension, and 60 microgram reduced cardiac output temporarily. During cardiopulmonary bypass, dogs treated with prostacyclin and heparin had low mean arterial perfusion pressures which responded to fluid infusion or phenylephrine. After 1 hour of cardiopulmonary bypass and reversal with protamine, dogs treated with prostacyclin and heparin had shorter bleeding times (p < 0.02) and better platelet function than control animals. After 2 hours, they had normal platelet number, but only half showed preservation of platelet function. When heparin was omitted, PGI2 preserved platelet number, but consumption coagulopathy developed, with prolonged prothrombin, partial thromboplastin, and bleeding times and decreased fibrinogen levels. PGI 2 preserves platelet number and function but may cause hypotension, and it cannot replace heparin in cardiopulmonary bypass.
J Thorac Cardiovasc Surg 1981 Feb
PMID:Preservation of platelet function and number by prostacyclin during cardiopulmonary bypass. 700 50

Thrombotic complications of percutaneous arterial catheterization still remain a significant and serious problem in infants and children. Systemic heparinization has been recommended for prevention of these complications. The purpose of this study was to evaluate the effect of intraarterial injection of heparin in reducing thrombotic complications following percutaneous femoral artery catheterization. One hundred sixteen consecutive patients (ages four months to 20 years) studied by the Desilets-Hoffman modification of Seldinger's technique of femoral artery catheterization were randomly allocated to the control or heparin groups using a double-blind technique. At the completion of the catheterization, 0.1 mg/kg of placebo or heparin (1,000 units/ml) was injected into the common iliac artery prior to removal of the catheter and sheath. Segmental plethysmography was performed in both lower extremities prior to and after the catheterization, and a plethysmography index (PI) was calculated. The age and sex distribution, diagnoses, number, type, and site of previous catheterization, hemoglobin, platelet count, the amount of flush solution and the heparin contained therein, size of the catheter and sheath used, number of arterial punctures, and the length of the time in the artery were similar in the two groups (P greater than 0.1). Thrombin time and activated partial thromboplastin time were measured prior to the use of flush solution and prior to angiography, and these remained essentially unchanged in the two groups. The PI in the control group (97.5 +/- 320 was not significantly different (P greater than 0.1) from that of the heparin group (97.7 +/- 32). Similarly, the six to 24 month of postcatheterization plethysmography data show no differences (P greater than 0.1). The number of patients with reduced ipsilateral posterior tibial and dorsalis pedis pulses was also similar (P greater than 0.1). None of the patients in either group required thrombectomy. The low low incidence of arterial complications in our patients when compared with other studies may be related in part to the use of a sheath, which is not called for in original Seldinger technique. The data suggest that full-dose heparin administration does not significantly alter arterial complications following percutaneous femoral artery catheterization, especially in children over five years of age.
Cathet Cardiovasc Diagn 1981
PMID:Effect of intraarterial injection of heparin on the complications of percutaneous arterial catheterization in infants and children. 702 38

Experimentally induced hypothermia (20 degrees C) for 60 minutes in dogs provokes a significant decrease in the platelet count, which reverses during subsequent rewarming, and the constant release of a heparin-like factor, which reacts as a specific inhibitor of factor Xa. This phenomenon is also rapidly reversible, and heparin values are not significantly different from control levels after 90 minutes of rewarming. The mean maximal concentration of heparin-like material is 0.54 U/ml, or about double control levels. Its half-life is approximately 90 minutes. The level of circulating antithrombin III was not modified during hypothermia and rewarming.
J Thorac Cardiovasc Surg 1981 Jul
PMID:In vivo release of a heparin-like factor in dogs during profound hypothermia. 724 30

The role of the platelet glycoprotein IIb/IIIa (GPIIb/IIIa) receptor and the efficacy of GPIIb/IIIa receptor antagonists on reocclusion after arterial versus venous thrombolysis is unknown. We used a canine model of simultaneous carotid artery and jugular vein thrombosis to evaluate the effect of the murine monoclonal antibody 7E3 [7E3 F(ab')2] on intravascular thrombotic reocclusion after thrombolysis in both vessels. The left carotid artery and right jugular vein were instrumented with flow probes, a critical stenosis, and an electrode through which an anodal current was applied to induce formation of an occlusive thrombus. After persistent occlusion of both vessels, 7E3 (0.8 mg/kg, n = 7) or saline (n = 10) was administered intravenously (i.v.) immediately after the local administration of anisolylated plasminogen streptokinase activator complex (APSAC, 0.1 U/kg). Ex vivo platelet aggregation in response to ADP or arachidonic acid was inhibited completely, and bleeding time was increased threefold by 7E3. The administration of 7E3 did not affect the activated partial thromboplastin time as compared with control values. The time to reperfusion of either vessel was not altered significantly in the presence of 7E3. Arterial or venous thrombolysis after APSAC was achieved in 10 of 10 and 8 of 10 control animals, respectively, but rethrombosis occurred in both the carotid artery and jugular vein in each of the saline-treated animals. Treatment with 7E3 prevented cyclic flow variations and reocclusion in the carotid artery (p < 0.05) in all treated animals (n = 7). In contrast, 7E3 did not suppress cyclic flow variations in the jugular vein, and rethrombosis occurred in five of six vessels despite the presence of platelet inhibition as assessed ex vivo. Residual arterial thrombus weights were reduced by pretreatment with 7E3 (saline = 24 +/- 4 mg, 7E3 = 11 +/- 3 mg; p < 0.05), whereas residual venous thrombus weights were not affected (saline 25 +/- 5 mg and 7E3 26 +/- 11 mg). The results indicate that inhibition of the platelet GPIIb/IIIa receptor does not prevent jugular vein rethrombosis despite its ability to prevent rethrombosis in the carotid artery. Different thrombotic mechanisms are involved in forming arterial and venous thrombi. Interventions that modulate arterial thrombotic events need not affect occlusive thrombotic activity in the venous circulation.
J Cardiovasc Pharmacol 1995 Aug
PMID:Monoclonal antibody [7E3 F(ab')2] prevents arterial but not venous rethrombosis. 747 49

Clinical pharmacology of the intravenously administered recombinant desulfatohirudin CGP 39393 was investigated in 47 healthy volunteers in a multicenter study. Mean peak concentrations after bolus injections of 0.1, 0.3, 0.5, and 1.0 mg/kg were 154, 443, 764, and 1,691 nmol/L, respectively. Intravenous infusions of 0.1 mg/kg/h for 6 h and of 0.2 and 0.3 mg/kg/h for 6 h and 72 h resulted in mean steady-state levels of 78, 227, and 312 nmol/L. Elimination was multiexponential and dose independent. Concordant pharmacokinetic parameters were obtained from both i.v. bolus and infusion experiments (overall average total plasma clearance, 2.20 ml/min/kg; mean residence time, 2.12 h; volume at steady state, 0.27 L/kg). Thrombin inhibition by CGP 39393 was demonstrated ex vivo by the thrombin chromogenic assay (TCA), by activated partial thromboplastin time (APTT), thrombin time (TT), and prothrombin time (PT). Following a parabolic function APTT doubled and quadrupled at CGP 39393 concentrations of 100 and 1,000 nmol/L, respectively. Whereas TTs (bovine thrombin 3 or 6 IU/ml) were very sensitive to low CGP 39393 levels with unmeasurable clotting times at CGP 39393 concentrations greater than 30 and 60 nmol/L, PT was prolonged by a factor of only 1.3 above baseline at 300 nmol/L. APTT appears to be most suitable for monitoring the anticoagulant effect of CGP 39393 over a broad concentration range. The drug was well tolerated without clinically relevant bleeding episodes or other adverse events.
J Cardiovasc Pharmacol 1993 Sep
PMID:Clinical pharmacology of intravenously administered recombinant desulfatohirudin (CGP 39393) in healthy volunteers. 750 25

We determined the effects of aspirin and a novel thromboxane A2/prostaglandin endoperoxide (TP)-receptor antagonist, BMS-180291, on thrombosis and bleeding times in skin and mesenteric arteries. In anesthetized rats, occlusive thrombosis was induced in the carotid artery by topical application of ferrous chloride and in the vena cava by blood flow stasis combined with either infusion of thromboplastin or hypotonic saline. Aspirin (1, 10, and 50 mg/kg) did not reduce arterial or venous thrombus weight significantly. BMS 180,291 (150 micrograms/kg/min) decreased arterial thrombus weight and hypotonic saline-induced caval thrombus weight by 58 and 57%, respectively. BMS-180291 lacked antithrombotic activity at a lower dose (50 micrograms/kg/min) and failed to inhibit thromboplastin-induced caval thrombosis. BMS-180291 (150 micrograms/kg/min) significantly reduced arterial thrombus weight by 40% when plasma epinephrine concentration was increased to 5 ng/ml. BMS-180291 and aspirin produced increases of only < or = 30% in bleeding times. These results demonstrate that BMS-180291 has antithrombotic activity in experimental aspirin-resistant arterial and venous thrombosis. Both aspirin and BMS-180291 have only modest effects on small artery hemostasis in rats.
J Cardiovasc Pharmacol 1993 Oct
PMID:Superior activity of a thromboxane receptor antagonist as compared with aspirin in rat models of arterial and venous thrombosis. 750 53

Thirty consecutive children scheduled for pediatric cardiac operation with cardiopulmonary bypass were included in the study. Before the operation, the patients were randomly divided into two groups: with aprotinin (n = 15, 30,000 U/kg after induction of anesthesia, 30,000 U/kg added to the prime of the cardiopulmonary bypass or without aprotinin (n = 15). Thrombomodulin, (free) protein S, protein C, and thrombin/antithrombin III complex were measured from arterial blood samples taken after induction of anesthesia (at baseline, before aprotinin) and before, during, and after cardiopulmonary bypass until the first postoperative day. Standard coagulation parameters (antithrombin III, fibrinogen, platelet count, and partial thromboplastin time) were without differences between the groups. Thrombomodulin plasma concentrations were within normal range ( < 40 micrograms/L) and were similar in both groups at baseline. During cardiopulmonary bypass and until 5 hours after cardiopulmonary bypass, however, thrombomodulin plasma levels were significantly lower in the children treated with aprotinin. No further differences were observed on the first postoperative day. Protein C and protein S plasma levels did not differ between the two groups. Thrombin/antithrombin III-complex plasma concentrations increased significantly during cardiopulmonary bypass, however, without showing differences between children with (225 +/- 49 micrograms/L) and without (149 +/- 31 micrograms/L) aprotinin treatment. Blood loss and the need for homologous blood and blood products did not differ significantly between the two groups. We concluded that administration of aprotinin resulted in reduced thrombomodulin plasma levels in pediatric patients undergoing cardiac operation without altering protein C/protein S plasma concentration. The exact role of aprotinin in endothelium-derived coagulation should be further studied.
J Thorac Cardiovasc Surg 1994 May
PMID:Influence of aprotinin on the thrombomodulin/protein C system in pediatric cardiac operations. 751 76


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